BACKGROUND Tbx5 deficiency in zebrafish causes several abnormal phenotypes of the heart and pectoral fins. It has been reported that exogenous human growth hormone can enhance expression of downstream mediators in the growth hormone and insulin-like growth factor I (IGF-I) pathway and partially restore dysmorphogenesis in tbx5 morphants. This study aimed to further evaluate the effects of IGF-I on cell apoptosis and dysmorphogenesis in zebrafish embryos deficient for tbx5. RESULTS Among the five studied groups of zebrafish embryos (wild-type embryos [WT], tbx5 morphants [MO], mismatched tbx5 morpholino-treated wild-type embryos [MIS], IGF-I-treated wild-type embryos [WTIGF1], and IGF-I-treated tbx5 morphants [MOIGF1]), the expression levels of the ifg1, igf1-ra, ifg-rb, erk1, and akt2 genes as well as the ERK and AKT proteins were significantly reduced in the MO group, but were partially restored in the MOIGF1 group. These expression levels remained normal in the WT, MIS, and WTIGF1 groups. Exogenous human IGF-I also reduced the incidence of phenotypic anomalies, decreased the expression levels of apoptotic genes and proteins, suppressed cell apoptosis, and improved survival of the MOIGF1 group. CONCLUSIONS These results suggest that IGF-I has an anti-apoptotic protective effect in zebrafish embryos with tbx5 deficiency.

中文翻译：

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IGF-1对tbx5缺陷斑马鱼胚胎的死亡率和畸形发生的抗凋亡作用。

背景技术斑马鱼中的Tbx5缺乏症会引起心脏和胸鳍的几种异常表型。据报道，外源性人类生长激素可以增强生长激素和胰岛素样生长因子I（IGF-1）途径中下游介质的表达，并部分恢复tbx5 morphant的畸形发生。这项研究旨在进一步评估IGF-I对缺乏tbx5的斑马鱼胚胎中细胞凋亡和畸形发生的影响。结果在五个研究斑马鱼胚胎组中（野生型胚胎[WT]，tbx5 morphant [MO]，错配的tbx5吗啉代处理的野生型[MIS]，IGF-I处理的野生型[WTIGF1]，和经IGF-I处理的tbx5突变体[MOIGF1]），ifg1，igf1-ra，ifg-rb，erk1，MO组中akt2和Akt2基因以及ERK和AKT蛋白明显减少，而MOIGF1组中部分恢复。这些表达水平在WT，MIS和WTIGF1组中保持正常。外源人IGF-I还减少了表型异常的发生率，降低了凋亡基因和蛋白质的表达水平，抑制了细胞凋亡，并提高了MOIGF1组的存活率。结论这些结果表明，IGF-I在tbx5缺乏的斑马鱼胚胎中具有抗凋亡保护作用。抑制细胞凋亡，并提高MOIGF1组的存活率。结论这些结果表明，IGF-I在tbx5缺乏的斑马鱼胚胎中具有抗凋亡保护作用。抑制细胞凋亡，并提高MOIGF1组的存活率。结论这些结果表明，IGF-I在tbx5缺乏的斑马鱼胚胎中具有抗凋亡保护作用。